Oral & Maxillofacial Surgery Review E-Book

Din Lam

• Herausgeber: Quintessence Publishing Co, Inc
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 511

Veröffentlichungsjahr: 2020

Beschreibung

This comprehensive text, prepared by experts in their field, provides a quick and effective way for both residents and busy clinicians to review important information and published literature in dentoalveolar surgery and implantology, anesthesiology, medicine, pathology, orthognathic surgery, craniofacial and reconstructive surgery, cosmetic surgery, and TMJ disorders and facial pain, as well as to gain new knowledge in these areas. The content is organized in bullet-point format and complemented by numerous illustrations, tables, and algorithms, making the material easy to remember. This is an excellent resource for board preparation as well as recertification. 187 illus.

Leseprobe

Oral and Maxillofacial Surgery Review: A Study Guide

Library of Congress Cataloging-in-Publication Data

Oral and maxillofacial surgery review : a study guide / edited by Din

Lam, Daniel Laskin.

      p. ; cm.

  ISBN 978-0-86715-674-4 (softcover)

  I. Lam, Din, editor. II. Laskin, Daniel M., 1924- , editor.

  [DNLM: 1. Oral Surgical Procedures--methods. WU 600]

  RK529

  617.5’22--dc23

  2015002883

© 2015 Quintessence Publishing Co, Inc

Quintessence Publishing Co Inc

4350 Chandler Drive

Hanover Park, IL 60133

www.quintpub.com

5 4 3 2 1

All rights reserved. This book or any part thereof may not be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise, without prior written permission of the publisher.

Editor: Bryn Grisham

Design and production: Kaye Clemens

Cover design: Ted Pereda

Printed in the USA

Contents

Preface

Contributors

1 Medical AssessmentAlia Koch and Steven M. Roser

2 AnesthesiaJason Jamali and Stuart Lieblich

3 Dentoalveolar SurgeryEsther S. Oh and George Blakey

4 Dental ImplantologyChristopher Choi and Daniel Spagnoli

5 Orthognathic SurgeryDavid Alfi and Jaime Gateno

6 TraumaDaniel E. Perez and Edward Ellis III

7 PathologyDin Lam and Eric R. Carlson

8 Maxillofacial ReconstructionDin Lam and Andrew Salama

9 Orofacial PainDavid W. Lui and Daniel M. Laskin

10 The TMJDavid W. Lui and Daniel M. Laskin

11 Craniofacial SurgeryJennifer Woerner and Ghali E. Ghali

12 Cosmetic SurgeryDavid E. Webb and Peter D. Waite

Index

Preface

When faced with a board or recertification examination, or just wanting to update your knowledge in oral and maxillofacial surgery, there is always the dilemma of where to begin and what and how much to study. This review book is designed to help you with this process. The format involves a detailed outline of the important items of didactic and clinical information in the 12 major areas of oral and maxillofacial surgery combined with numerous tables, summary charts, and useful mnemonics and surgical tips. Each chapter is also supplemented with many clinical photographs, diagrams, and photomicrographs, where appropriate.

The various chapters were each developed by two authors: (1) a young oral and maxillofacial surgeon who was board certified in recent years and is therefore very familiar with the process and the content, and (2) a more senior surgeon who has been a board examiner and/or involved in the recertification process and is therefore knowledgeable and experienced in the essential clinical aspects of the specialty.

To use this book as a review or study guide, it is suggested that you first read each chapter to determine what information is already familiar to you, what is new and needs to be learned, and what are the areas in which you desire more information from other sources such as the list of recommended reading at the end of each chapter. The last material should then be annotated where indicated in the various chapters. The book now becomes your study manual as well as a quick and easy way to review the material again just prior to the examination and a handy reference source during clinical practice.

We would like to express our deep appreciation and thanks to all of the contributing authors who gave so freely of their time and knowledge and who helped make this book a reality. Finally, we would like to thank Lisa Bywaters and Bryn Grisham of Quintessence Publishing for their expertise and guidance during the editorial process. Their concern for the success of this book was no less than ours.

Contributors

David Alfi,DDS, MD

Attending Oral and Maxillofacial Surgeon

Department of Oral and Maxillofacial Surgery

Houston Methodist Hospital

Houston, Texas

Assistant Professor of Clinical Surgery

Weill Cornell Medical College

Cornell University

New York, New York

George Blakey,DDS

Director of Oral and Maxillofacial Surgery Residency Program

Distinguished Associate Professor

Department of Oral and Maxillofacial Surgery

School of Dentistry

University of North Carolina

Chapel Hill, North Carolina

Eric R. Carlson,DMD, MD

Professor and Kelly L. Krahwinkel Chair

Department of Oral and Maxillofacial Surgery

Director of Oral and Maxillofacial Surgery Residency Program

University of Tennessee Graduate School of Medicine

Director of Oral/Head and Neck Oncologic Surgery Fellowship Program

Cancer Institute

University of Tennessee Medical Center

Knoxville, Tennessee

Christopher Choi,DDS, MD

Private Practice Limited to Oral and Maxillofacial Surgery

Rancho Cucamonga, California

Assistant Professor

Department of Oral and Maxillofacial Surgery

School of Dentistry

Loma Linda University

Loma Linda, California

Edward Ellis III,DDS, MS

Professor and Chair

Department of Oral and Maxillofacial Surgery

School of Dentistry

University of Texas Health Science Center at San Antonio

San Antonio, Texas

Jaime Gateno,DMD, MD

Chair, Department of Oral and Maxillofacial Surgery

Houston Methodist Hospital

Houston, Texas

Professor of Clinical Surgery

Weill Cornell Medical College

Cornell University

New York, New York

Ghali E. Ghali,DDS, MD

Professor and Chairman

The Jack W. Gamble Chair

Department of Oral and Maxillofacial Surgery

Louisiana State University Health Sciences Center—Shreveport

Shreveport, Louisiana

Jason Jamali,DDS, MD

Clinical Assistant Professor

Department of Oral and Maxillofacial Surgery

College of Dentistry

University of Illinois at Chicago

Chicago, Illinois

Alia Koch,DDS, MD

Assistant Professor

Department of Oral and Maxillofacial Surgery

College of Dental Medicine

Columbia University

New York, New York

Attending Oral and Maxillofacial Surgeon

New York Presbyterian Hospital

Columbia University Medical Center

New York, New York

Din Lam,DMD, MD

Adjunct Assistant Professor

Department of Oral and Maxillofacial Surgery

School of Dentistry

Virginia Commonwealth University

Richmond, Virginia

Daniel M. Laskin,DDS, MS

Professor and Chairman Emeritus

Department of Oral and Maxillofacial Surgery

School of Dentistry

Virginia Commonwealth University

Richmond, Virginia

Stuart Lieblich,DMD

Clinical Professor

Department of Oral and Maxillofacial Surgery

School of Dental Medicine

University of Connecticut

Farmington, Connecticut

Private Practice Limited to Oral and Maxillofacial Surgery

Avon, Connecticut

David W. Lui,DMD, MD

Assistant Professor

Department of Oral and Maxillofacial Surgery

School of Dentistry

Virginia Commonwealth University

Richmond, Virginia

Esther S. Oh,DDS, MD

Clinical Assistant Professor

Department of Oral and Maxillofacial Surgery

College of Dentistry

University of Florida

Gainesville, Florida

Daniel E. Perez,DDS

Associate Professor

Department of Oral and Maxillofacial Surgery

School of Dentistry

University of Texas Health Science Center at San Antonio

San Antonio, Texas

Steven M. Roser,DMD, MD

DeLos Hill Professor and Chief

Division of Oral and Maxillofacial Surgery

Department of Surgery

Emory University School of Medicine

Atlanta, Georgia

Andrew Salama,DMD, MD

Assistant Professor, Department of Oral and Maxillofacial Surgery

Director, Advanced Specialty Education Program in Oral and Maxillofacial Surgery

Henry M. Goldman School of Dental Medicine

Boston University

Boston, Massachusetts

Daniel Spagnoli,DDS, MS, PhD

Associate Professor and Chairman

Department of Oral and Maxillofacial Surgery

School of Dentistry

Louisiana State University Health Sciences Center—New Orleans

New Orleans, Louisiana

Peter D. Waite,DDS, MD, MPH

Professor and Chairman

Department of Oral and Maxillofacial Surgery

School of Dentistry

University of Alabama at Birmingham

Birmingham, Alabama

David E. Webb, Maj. USAF, DC

Attending Oral and Maxillofacial/Head and Neck Surgeon

Department of Oral and Maxillofacial Surgery

David Grant USAF Medical Center

Travis AFB, California

Jennifer Woerner,DMD, MD

Assistant Professor and Fellowship Director

Craniofacial and Cleft Surgery

Department of Oral and Maxillofacial Surgery

Louisiana State University Health Sciences Center—Shreveport

Shreveport, Louisiana

Chapter 1

Medical Assessment

Alia Koch and Steven M. Roser

Cardiovascular DiseaseRespiratory DiseaseRenal DiseaseAcid-Base DisordersGastrointestinal DiseaseHematologic DiseaseEndocrine DiseaseAutoimmune DiseaseNeurologic DisordersPerioperative Management

Cardiovascular Disease

Acute Coronary Syndrome

Major blood vessels supplying the heart are damaged/diseased by cholesterol plaques, which cause the vessels to narrow. In turn, less blood reaches the myocardium, leading to an acute coronary syndrome.

•Symptoms: Dull substernal pain and pain radiating to left arm and jaw; associated with diaphoresis, dyspnea

•Diagnosis: electrocardiogram (ECG), cardiac enzymes

– ST segment elevation myocardial infarction (STEMI)

∘ Treatment: Immediate reperfusion (angioplasty or thrombolytic therapy) within 12 hours of onset of chest pain

– Non-ST segment elevation myocardial infarction (NSTEMI)

∘ Treatment: Medical therapy (aspirin, beta blockade, angiotensin-converting enzyme [ACE] inhibitor)

– Unstable angina

∘ Treatment: Medical therapy (same as NSTEMI)

Congestive Heart Failure

• Systolic heart failure: Reduced ejection fraction (< 40%), S3 murmur, dilated left ventricle

• Diastolic heart failure: Preserved ejection fraction (> 50%), S4 murmur, left ventricle hypertrophy

•Symptoms: Chest pain, shortness of breath, orthopnea, extremity swelling, jugular vein distention

•Diagnosis

– Echocardiogram: Evaluate heart motion, ejection fraction

– ECG: Evaluate changes in ECG, heart strain

– Stress test: Evaluate coronary artery disease

– Brain natriuretic peptide: Normal value rules out acute heart failure

– Chest radiograph: Evaluate heart size, fluid in the intrathoracic cavity

Classification of congestive heart failure (CHF)

Stage

Definition

Treatment

A

Risk of HF due to comorbidities only

Treat underlying condition

B

No symptoms but structural abnormality predisposes patient to HF

ACE inhibitor, beta blocker

C

Structural disease with HF symptoms

ACE inhibitor, beta blocker, diuretic, salt restriction

D

HF symptoms at rest

Medical therapy with mechanical support

HF, heart failure.

Valvular Disease

Arrythmias

CHADS2 scoring table

Stroke risk assessment in atrial fibrillation to determine necessity of anticoagulation or antiplatelet treatment.

Condition

Points

C

Congestive heart failure

1

H

Hypertension: Blood pressure consistently above 140/90 mm Hg (or treated hypertension with medication)

1

A

Age ≥ 75 years

1

D

Diabetes mellitus

1

S2

Prior stroke or transient ischemic attack (TIA) or thromboembolism

2

Stroke risk assessment

Score

Risk

Treatment

0

Low

Aspirin or none

1

Moderate

Aspirin or coumadin to INR of 2-3

2 or more

Moderate/high

Coumadin to INR of 2 to 3

INR, international normalized ratio.

Heart block (Fig 1-1)

Fig 1-1 Heart block ECG strips. (a) First degree. (b) Second degree, type 1. (c) Second degree, type 2. (d) Third degree. P waves indicated by a red vertical line. (Reprinted with permission from EKG-Uptodate 2013.)

ECG finding

Treatment

Type 1

Increased PR Interval

None

Type 2A

Increasing PR interval until dropped QRS

Pacemaker for symptomatic patients only

Type 2B

Regularly dropped QRS with constant PR interval

Search for cause/pacemaker

Type 3

Complete dissociation of P waves and QRS complexes

Search for cause/pacemaker

Hypertension

• Primary hypertension: No identifiable cause

• Secondary hypertension: Identifiable cause, some listed below

– Renal artery stenosis

– Diabetic nephropathy

– Thyroid disease

– Cocaine use

– Pheochromocytoma

– Obstructive sleep apnea

•Diagnosis: At least two elevated BP readings on at least two different occasions

– Prehypertension: Systolic blood pressure (SBP) from 120 to 130 mm Hg, diastolic blood pressure (DBP) from 80 to 89 mm Hg

– Stage 1: SBP from 140 to 159 mm Hg, DBP from 90 to 99 mm Hg

– Stage 2: SBP ≥ 160 mm Hg, DBP ≥ 100 mm Hg

•Etiology: Obesity, familial, smoking, diabetes, kidney disease, Cushing syndrome, catecholamines, obstructive sleep apnea

•Treatment: Diet, weight reduction, aerobic activity, sodium restriction, medications

Medications

Hypertensive emergencies

Infective Endocarditis (IE)

Type

Cause

IV drug use

Staphylococcus aureus

Native valve

Viridans streptococci, S aureus, enterococci

Prosthetic valve

Staphylococcus epidermidis, S aureus

Culture negative

HACEK organism (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella corrodens, Kingella), Candida, Aspergillus

IV, intravenous.

Duke criteria for diagnosis

• Definite IE: 2 major; 1 major and 3 minor; 5 minor

• Possible IE: 1 major and 1 minor; 3 minor

Major criteria

Minor criteria

• Positive blood culture

• Echocardiogram with evidence of endocardial involvement

• Predisposition to IE (IV drug use, indwelling catheter, diabetes)

• Fever

• Vascular phenomena (Janeway lesions, arterial emboli, intracranial hemorrhage, splinter hemorrhage)

• Microbiologic evidence

• Immunologic phenomena (Osler nodes, Roth spots)

IV, intravenous.

Treatment

• Native valve endocarditis: Vancomycin and gentamicin

• Prosthetic valve endocarditis: Vancomycin, rifampin, and gentamicin

• Culture positive: Treat organism

Surgical Management of Patients on Cardiovascular Medications

Preoperative treatment decision algorithm

1. Urgent surgery, nonurgent surgery with unstable/active cardiac condition

• Medical consult/discussion with surgeon

2. Nonurgent surgery

• Surgical procedure risk (Box 1-1)

– Low risk: Medical consult preoperatively

– Moderate/high risk: Go to step 3

3. Evaluate patient’s functional capacity (Box 1-2)

• > 4 METs: Statin therapy and beta blocker preoperatively

• ≤ 4 METs: Go to step 4

4. Evaluate risk of surgical procedure (see Box 1-1)

• Moderate risk: Statin, beta blocker, ECG, possible ACE inhibitor

• High risk: Go to step 5

5. Evaluate cardiac risk factors (Box 1-3)

• ≤ 2: Preoperative statin, beta blocker, possible ACE inhibitor

• > 2: Noninvasive testing, discuss anesthesia technique, consider changing surgical management

MET, metabolic equivalent of task.

Box 1-1 Risk of surgical procedures

Low risk

Intermediate risk

High risk

Dental

Eye

Gynecologic

Breast

Minor genitourinary

Head and neck

Transplant

Major genitourinary

Intraperitoneal

Intrathoracic

Open heart

Vascular

Box 1-2 Assessment of functional capacity

Metabolic equivalents of task (METs) are a physiologic measurement that expresses the energy associated with physical activities.

1 MET

• Can you take care of yourself?

• Can you walk indoors?

• Can you feed yourself?

• Can you dress yourself?

• Can you walk 1 to 2 blocks?

4 METs

• Can you climb a flight of stairs?

• Can you do heavy housework?

• Can you participate in moderate recreational activities?

> 10 METs

• Can you participate in strenuous sports?

Box 1-3 Cardiac risk factors

• History of angina

• History of myocardial infarction

• History of heart failure

• History of stroke

• Diabetes mellitus

• Renal failure

Respiratory Disease

Normal Lung Volumes (Figs 1-2 and 1-3)

Fig 1-2 Lung volumes and capacities. IRV, inspirational reserve capacity; TV, tidal volume; ERV, expiratory reserve volume; RV, residual volume; IC, inspirational capacity; FRC, functional residual capacity; TLC, total lung capacity; VC, vital capacity.

Fig 1-3 Flow volume curves. (Reprinted with permission from Levitzky MG. Pulmonary Physiology, 7 ed. New York: McGraw-Hill, 2007.)

Common abbreviations

• Residual volume (RV): Air left after maximal expiration

• Tidal volume (TV): Entering air during normal inspiration

• Expiratory reserve volume (ERV): Air that can still be expired after normal expiration

• Functional residual capacity (FRC): RV + ERV

Abbreviations associated with pulmonary function tests (PFTs)

• Forced expiratory volume in 1 second (FEV1): Air that can be expired in 1 second

• Forced vital capacity (FVC): Maximum volume of air that can be forcefully exhaled

• Total lung capacity (TLC): FVC + RV

Common types of pulmonary disease

Obstructive

Restrictive

Extraparenchymal restrictive

• Asthma

• Cystic fibrosis

• Chronic obstructive pulmonary disease (COPD)

• Sarcoidosis

• Interstitial lung disease

• Collagen disorder

• Obesity

• Scoliosis

• Myasthenia gravis

• Diaphragmatic weakness

• Cervical spine injury

Obstructive versus restrictive lung disease

Obstructive

Restrictive

FEV1

Decreased

Decreased

FVC

Normal

Decreased

FEV1/FVC

Decreased

Normal/increased

Lung volume

Increased

Decreased

Flow rates

Decreased

Decreased

Chronic Respiratory Diseases

Asthma

•Definition: Chronic obstructive reversible disorder of airway hyper-reactivity causing dyspnea, cough, wheezing, and chest tightness

•Diagnosis: Diagnosed by showing reversible obstructive lung disease with normal diffusing capacity

• Exam will show expiratory wheezing during acute exacerbations, with a prolonged expiratory phase

• Severe attacks will have pulsus paradoxus, accessory muscle use, and silent chest

Definition

Treatment

Mild intermittent

< 2 days/week with PEF > 80%

Bronchodilator as needed

Mild persistent

> 2 days/week but < 1 time/day with PEF > 80%

Low-dose inhaled steroids

Moderate persistent

Daily symptoms with PEF between 60% and 80%

Inhaled steroids and long-acting beta 2 agonist

Severe persistent

Continuous symptoms with PEF < 60%

Add oral steroids

PEF, peak expiratory flow.

Medications for treatment of asthma

Mechanism of action

Example

Beta 2 agonist

Beta 2 agonism causes an increase in cAMP formation leading to relaxation of bronchial muscle

Albuterol, salmeterol

Corticosteroids

Suppresses inflammatory response and decreases mucosal edema

Fluticasone, hydrocortisone, prednisolone

Leukotriene modifier

Leukotriene receptor antagonist decreases bronchoconstriction

Montelukast

5-Lipoxygenase

Inhibits leukotriene formation

Zileuton

Anticholinergic

Blocks cholinergic constriction causing bronchodilation

Ipratropium bromide

cAMP, cyclic adenosine monophosphate.

Chronic Obstructive Pulmonary Disease (COPD)

•Definition: Nonreversible chronic airway restriction

•Symptoms: Worsening dyspnea, increasing cough and change in sputum, hyperinflation, prolonged expiration, wheezing

• Chronic bronchitis: Chronic productive cough for 3 months in 2 consecutive years; “blue bloater”

• Emphysema: Enlargement of airways and wall destruction distal to bronchioles; “pink puffer;” pursed-lip breathing

•Diagnosis:

– PFTs to evaluate FEV1, FEV1/FVC, and postbronchodilator values

– Arterial blood gas (ABG) analysis will show hypercarbia, hypoxemia

– Evaluate for alpha 1 antitrypsin deficiency in emphysema patients

– Chest radiograph

Classification of COPD

Stage

FEV1

Treatment

1

> 80

Short-acting bronchodilator (albuterol)

2

50–79

Long-acting B2 agonist (salmeterol) and anticholinergic bronchodilator (ipratropium)

3

30–49

Inhaled steroid

4

< 30

Oxygen, pulmonary rehabilitation, consider transplant in worst cases

Acute Pulmonary Diseases

Acute respiratory distress syndrome (ARDS)

•Definition: Acute, hypoxemic respiratory failure associated with bilateral lung infiltrates

•Etiology: Pneumonia, aspiration, trauma, acute pancreatitis, inhalational injury, reperfusion injury

•Symptoms: Rapid onset of dyspnea, tachypnea, diffuse lung crackles

•Diagnosis: Bilateral infiltrates on chest radiograph, ratio of PaO2 to FiO2 < 200

•Treatment

– Treat underlying cause

– Use mechanical ventilation with low tidal volumes of 6 cc/kg

– Positive end-expiratory pressure (PEEP)

– Conservative fluid management

Pulmonary embolus (PE)

•Risk factors: Prior PE, pregnancy, malignancy, obesity, immobility, stroke, tobacco use, recent surgery, trauma

•Symptoms: Dyspnea, hemoptysis, fever, cough, tachypnea, tachycardia

•Diagnosis

– Modified Wells criteria (see table below)

– D-dimer test: Only helpful to exclude PE in low-risk patients (Wells score ≤ 4)

– Computed tomography angiography (CTA): Multidetector-row CTA (MDCTA) is standard pulmonary angiography when CTA is not available

– ECG: New right heart strain; nonspecific anterior T wave inversions; sinus tachycardia; large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III (S1Q3T3)

– ABG analysis: Respiratory alkalosis with increased alveolar arterial gradient

– V/Q scan: Ventilation without perfusion suggests PE

•Treatment

– Heparin as bridge to coumadin to maintain INR of 2 to 3 for at least 3 to 6 months

– Inferior vena cava filter if anticoagulation is contraindicated

– Direct thrombin inhibitors for patients with heparin-induced thrombocytopenia (HIT)

– Thrombolysis for massive PE

– Thrombectomy

Modified Wells criteria

To determine likelihood of PE.

Criteria

Points

Clinical signs and symptoms of DVT

3

PE is primary diagnosis

3

Heart rate > 100 bpm

  1.5

Immobilized for at least 3 days or surgery in previous 4 weeks

  1.5

Previous objectively diagnosed PE or DVT

  1.5

Malignancy with treatment within 6 months or palliation

1

Hemoptysis

1

DVT, deep vein thrombosis.

Contraindications to anticoagulation

Relative

Absolute

• Thrombocytopenia

• Prior hemorrhagic stroke

• Recent internal bleeding

• Active internal bleeding

• Aortic dissection

• Active hemorrhagic stroke

Renal Disease

Acute Renal Failure

• Increase in serum creatinine ≥ 0.3 mg/dL over baseline

• Urine output less than 0.5 cc/kg/hour for more than 6 to 12 hours

Prerenal

•Etiology: Volume depletion, severe liver disease, severe CHF

•Diagnosis: Fractional excretion of sodium (FENa) < 1%; ratio of blood urea nitrogen (BUN) to creatinine, 10–15:1; high urinary osmolarity

•Treatment: Fluids (rapid improvement with fluids)

Renal

•Etiology: Tubular injury, acute tubular necrosis, interstitial disease, glomerular disorder

•Diagnosis: FENa >1%; BUN-to-creatinine ratio, 10–15:1; muddy brown casts

•Treatment: Remove underlying agent, treat underlying cause

Postrenal

•Etiology: Urinary tract obstruction

•Diagnosis: FENa < 1%, oliguria/anuria

•Treatment: Remove obstruction

Need for emergent dialysis

A

Acidosis

E

Electrolyte abnormality

I

Ingestion

O

Overload

U

Uremia

Chronic Renal Failure (CRF)

• Permanent loss of renal function for at least 3 months

•Etiology: Hypertension, diabetes, renal artery stenosis, polycystic kidney disease

•Diagnosis: Glomerular filtration rate (GFR) < 15 mL/minute, albuminuria > 30 mg/day

•Treatment: Management of hypertension with ACE inhibitors and angiotensin receptor blockers, low density lipoproteins < 100 mg/dL

• Predictor of disease progression: Proteinuria

Severity of chronic renal disease based on GFR

GFR stage

GFR (mL/min/1.73 m2)

Kidney function

G1

> 90

Normal

G2

60–89

Mildly decreased

G3a

45–59

Mild to moderately decreased

G3b

30–44

Moderately to severely decreased

G4

15–29

Severely decreased

G5

< 15

Kidney failure

G5D

< 15

Kidney failure treated with dialysis

Severity of chronic renal disease based on albuminuria

Albuminuria stage

Albumin excretion rate (mg/day)

Albumin excretion

A1

< 30

Normal to increased

A2

30–300

Moderately increased

A3

> 300

Severely increased

Complications of CRF

Treatment

Anemia

Erythropoietin injections, iron

Renal osteodystrophy

Phosphate binder

Hyperkalemia

Dietary restriction, diuretic

Acidosis

Sodium bicarbonate

Pericarditis

Dialysis

Dialysis infections

Antibiotics, catheter removal

Urinalysis interpretation

Nephrotic Disease

•Symptoms: Peripheral edema, hypoalbuminemia, hyperlipidemia, increased proteinuria

•Diagnosis: Urinalysis shows oval fat bodies, proteinuria, and 24-hour urine protein > 3.5 g/day

Primary nephrotic syndrome

Direct damage to glomeruli causing massive proteinuria.

Primary disease

Pathology

Treatment

Membranous nephropathy

Thickening of capillary loops with subepithelial deposits

ACE inhibitor, steroid

Focal segmental glomerulosclerosis

Glomerulosclerosis

Steroids, cyclosporine

Goodpasture syndrome

Linear IgG deposition along glomerular basement membrane

Steroids, cyclophosphamide, plasmapheresis

Minimal change disease

Epithelial foot process loss

Steroids

IgG, immunoglobulin G.

Secondary nephrotic syndrome

Damage of glomeruli secondary to systemic disease.

Pathology

Treatment

Diabetes mellitus

Kimmelstiel-Wilson lesion

Glucose, lipid, blood pressure control, ACE inhibitor, angiotensin receptor blocker

Multiple myeloma

Light chain involvement with positive Congo red stain

Treatment of systemic disease

Amyloidosis

Amyloid deposition with positive Congo red stain

Treatment of systemic disease

Nephritic Disease

Inflammatory disorder in the glomeruli.

• Glomerulonephritis: RBCs in urine with or without cellular casts and varying degrees of proteinuria

•Symptoms: Hypertension, edema, oliguria, hematuria

•Diagnosis: Red blood cell (RBC) casts in urine, renal biopsy

• Types of glomerulonephritis

– Immune complex: Decreased complement levels

– Pauci immune: Normal complement levels

Immune complex glomerulonephritis

Pathology

Treatment

Subacute bacterial endocarditis

Crescent glomerulonephritis

Antibiotics

Post-streptococcal

Subepithelial humps

Resolves after treatment of streptococcal infection

Membranoproliferative

glomerulonephritis

Subendothelial deposits

Treat cryoglobulinemia

Pauci immune glomerulonephritis

Pathology

Treatment

IgA nephropathy

IgA deposits in mesangium

ACE inhibitor/angiotensin receptor blocker, steroids

Wegener granulomatosis

Necrotizing crescent disease

Steroids, cyclophosphamide

Churg-Strauss syndrome

Necrotizing crescent disease

Steroids, cyclophosphamide

IgA, immunoglobulin A.

Nephrotic Versus Nephritic Disease

Nephrotic

Nephritic

Protein

Very large amount

Small amount

Urinalysis

No casts but will find lipid-laden macrophages and free lipid

Abundant RBCs and RBC casts; no lipids seen

BP

Mildly elevated or normal

Severely elevated

GFR

Normal

Elevated

BP, blood pressure.

Acid-Base Disorders

Arterial Blood Gas (ABG) Versus Venous Blood Gas (VBG)

• ABG: The gold standard to evaluate acid-base disorders

– Invasive procedure

– Serial examinations necessary

– Risk of hematoma and nerve injury

• VBG

– Easier to obtain and less injury to patients

– Data (pH, bicarbonate [HCO3], lactate, and base excess) are similar to those found in ABG

– Partial pressure of carbon dioxide (PaCO2) is also well correlated except in patients with severe shock or when PaCO2 > 45 mm Hg

Quick Guide to ABG Interpretation

Step one: Identify primary disorder

• Evaluate pH and PaCO2:

– If change in same direction → metabolic disorder

– If change in different direction → respiratory disorder

Primary disorder

Primary change

Compensatory change

Metabolic acidosis

Decreased HCO3

Decreased PaCO2

Metabolic alkalosis

Increased HCO3

Increased PaCO2

Respiratory acidosis

Increased PaCO2

Increased HCO3

Respiratory alkalosis

Decreased PaCO2

Decreased HCO3

Step two: Check for compensation if disorder has a primary origin

• Metabolic disorder: Calculate the expected PaCO2

• Respiratory disorder: Calculate the expected pH

• If the actual value is different from the calculated value (pH or PaCO2), expect an additional acid-base disorder

Step three: Calculate the anion gap if metabolic acidosis or mixed disorder is detected

• Anion gap (AG): Na – (Cl + HCO3) ≤ 12

• If AG < 12, acidosis is due to loss of bicarbonate (ie, diarrhea)

• If AG > 12, acidosis is due to increase of nonvolatile acids (ie, lactic acidosis)

• AG can be influenced by an abnormal albumin level

Acid-Base Disorders

Metabolic acidosis

Decreased blood pH with decreased bicarbonate

Etiology: Two types

• AG > 12: “MUDPILES”

–Methanol ingestion

–Uremia

–Diabetic ketoacidosis

–Paraldehyde Ingestion

–Isoniazid ingestion

–Lactic acidosis

–Ethylene glycol ingestion

–Salicylate ingestion

• Non-AG

– Gastrointestinal losses: Diarrhea, small bowel fistula, pancreatic fistula

– Renal loss: Renal tubular acidosis

Signs/Symptoms

• Hyperventilation (compensatory mechanism)

• Decreased tissue perfusion

• Decreased cardiac output

• Altered mental status

• Arrhythmias

• Hyperkalemia

Treatment

• Treat underlying cause

– Most of the time acidosis is not harmful

– Cause of death in these patients due to underlying condition rather than acidemia

• Sodium bicarbonate

– Has shown to be ineffective therapy in management of acidosis

– Only use in patients who are deteriorating rapidly

Metabolic alkalosis

Increased blood pH with increased bicarbonate

Etiology

• Extracellular fluid expansion

– Adrenal disorders causing increased mineralocorticoid secretion; increased reabsorption of bicarbonate and sodium and secretion of chloride

• Extracellular fluid contraction

– Vomiting, nasogastric suction causing hydrochloric acid and bicarbonate loss

– Excessive use of diuretics

Signs/Symptoms

• Hypokalemia

• Elevated bicarbonate

• Elevated pH

• Hypoventilation

• Arrhythmias

• Decrease in cerebral blood flow

Treatment

• Treat underlying cause

• Volume-depleted patient requires normal saline with potassium replacement

• In the volume-overloaded patient, consider spironolactone

Respiratory acidosis

Alveolar hypoventilation: Decreased blood pH with arterial PaCO2 > 40

• Acute: No renal compensation

• Chronic: Renal compensation with increase in plasma bicarbonate

Etiology

• Chronic obstructive pulmonary disease

• Brainstem injury

• Respiratory muscle fatigue

• Drug overdose causing hypoventilation

Signs/Symptoms

• Confusion

• Headaches

• Fatigue

• Central nervous system (CNS) depression

Treatment

• Supplemental oxygen

• Treat underlying disorder

• Consider mechanical ventilation with severe acidosis, deteriorating mental status, and impending respiratory failure

Respiratory alkalosis

Alveolar hyperventilation: Increased blood pH with decrease in PaCO2

• Acute renal compensation: For every 10 mm Hg decrease in PaCO2, bicarbonate will decrease by 2

• Chronic renal compensation: For every 10 mm Hg decrease in PaCO2, bicarbonate will decrease by 5

Etiology

• Anxiety

• Sepsis

• Pregnancy

• Liver disease

• Pulmonary embolism

• Asthma

Signs/Symptoms

• Decreased cerebral blood flow

• Lightheadedness

• Anxiety

• Perioral numbness

• Arrhythmias

Treatment

• Treat underlying disorder

• Inhale CO2 (breathing into a paper bag)

Sodium Disorders

• Normal sodium concentration in the body is 135 to 145 mEq/L

• To determine the cause of sodium disorder, measure

– Plasma osmolality (290 mOsm/kg H2O)

∘ (2 × Plasma Na+) + Glucose/18

– Extracellular volume

∘ Clinical examination (eg, peripheral edema, orthostatic hypotension, and skin turgor)

∘ Not the most reliable method but is readily available

∘ Invasive monitoring (cardiac filling pressures and cardiac output)

Potassium Disorders

• Normal potassium level is between 3.5 mEq/L and 5 mEq/L

• Work-up should include:

– Urine potassium and chloride level

– Serum magnesium level

– ABG as needed

Hypokalemia

Hypokalemia is better tolerated than hyperkalemia

Etiology

• Nonrenal: Urine potassium < 30 mEq/L; diarrhea

• Renal loss: Urine potassium > 30 mEq/L

– High urine chloride (> 25 mEq/L)

∘ Magnesium depletion

∘ Diuretic

– Low urine chloride (< 25 mEq/L)

∘ Nasogastric suctioning

∘ Alkalosis

Symptoms

• Mild hypokalemia (2.5 to 3.5); can be asymptomatic

• Severe hypokalemia (< 2.5 mEq/L); diffuse muscle weakness

• Abnormal ECG; prominent U waves, flattening and inversion of T waves, and QT prolongation

• Only occurs in 50% of cases

Treatment

• Treat underlying cause

• Magnesium replacement

• Potassium (KCl) replacement should be done gradually

– Oral replacement in mild cases

– Intravenous (IV) replacement in cases with arrhythmia; increase no greater than 20 mEq/L

Hyperkalemia

Poorly tolerated, especially when level is above 5.5 mEq/L; a patient with chronic renal disease may normally have an elevated potassium level

Etiology

• Nonrenal (transcellular shift)

– Acidosis

– Rhabdomyolysis

• Impaired renal excretion

– Adrenal insufficiency

– Drug (eg, potassium-sparing diuretics)

– Renal insufficiency

Symptoms

• ECG changes

– Begins to change when potassium reaches 6 mEq/L

– Stages

∘ 1st stage: Peaked T waves (V2 and V3)

∘ 2nd stage: Flattened P waves and PR interval lengthening

∘ 3rd stage: Disappearance of P waves and QRS prolongation

∘ Final: Ventricular asystole

• Respiratory failure

• Nausea/vomiting

• Muscle weakness

Treatment

• ECG changes: IV calcium gluconate to decrease cardiac excitability

• Shift potassium from extracellular to intracellular with insulin and dextrose

• Diuretics, exchange resins (kayexalate), dialysis to remove potassium

Gastrointestinal Disease

Irritable Bowel Syndrome

Crohn disease

Ulcerative colitis

Definition

Chronic disease with patchy transmural inflammation

Chronic disease with diffuse and continuous mucosal inflammation

Symptoms

Nonbloody diarrhea, low-grade fever, pain, malaise, weight loss

Bloody diarrhea, fecal urgency, fever, uveitis, erythema nodosum, anklyosing spondylitis

Location

Anywhere in the gastrointestinal tract with propensity for the ileum

Colon to the rectum

Diagnosis

Colonoscopy with biopsy

Colonoscopy with biopsy, stool studies, abdominal radiograph showing lead pipe appearance of colon with loss of haustrations

Malignancy potential

Questionable increased malignancy risk

Increased malignancy risk

Treatment

Steroid, immunomodulatory drugs, 5-aminosalicylic acid

Mesalamine, steroid, surgery

Hepatitis

Hepatitis B serology

Gastroesophageal Reflux Disease

•Etiology: Lower esophageal sphincter relaxation

•Symptoms: Retrosternal burning, regurgitation, excessive salivation, bitter test, throat fullness, halitosis

•Diagnosis: Treat empirically; if no success, upper endoscopy with biopsy, esophageal pH monitoring

•Treatment: Elevate head of bed, stop tobacco and alcohol use, dietary modification, antacids, histamine blockers, proton pump inhibitors

•Complications: Barrett esophagus, adenocarcinoma, upper gastrointestinal bleeding, cough, asthma

End Stage Liver Disease (ESLD)

•Etiology: Chronic hepatocellular injury leads to fibrosis of liver

•Symptoms: Fatigue, anorexia, impotence, melena, spider nevi, gynecomastia, jaundice, testicular atrophy, coarse hand tremor, caput medusae, spider telangiectasia, Dupuytren contractures

•Diagnosis: Liver function tests, liver biopsy; monitor disease with Child-Turcotte-Pugh score or model for end stage liver disease (MELD) score

•Treatment: Avoid alcohol and medications metabolized by the liver, treat underlying disease process, screen for hepatocellular carcinoma, monitor for complications

•Complications: Esophageal varices, ascites, increase in bleeding risk, portal hypertension, hepatic encephalopathy

Child-Turcotte-Pugh score

• 5 to 6 points: Class A, 90% 3-year survival rate

• 7 to 9 points: Class B, 50% to 60% 3-year survival rate

• > 9 points: Class C, 30% 3-year survival rate

Hematologic Disease

Anemia

Hypoproliferative (low reticular cell count)

Hyperproliferative (high reticular cell count)

Sickle Cell Disease

Homozygous defect in gene for beta-globulin that produces hemoglobin S.

•Triggers: Dehydration, acidosis, hypoxia

•Diagnosis: Target cells, sickle cells, Howell Jolly bodies, hemoglobin S on smear

•Symptoms: Acute chest pain, stroke, autosplenectomy

•Treatment: Folate, hydroxyurea, aggressive hydration, analgesia, oxygen, transfuse for major surgery (9 to 10 g hemoglobin)

Acute complications

Chronic complications

• Stroke

• Splenic infarct

• Osteomyelitis

• Retinopathy

• Avascular necrosis of the hip

• Chronic renal failure

Bleeding Disorders

Disseminated Intravascular Coagulation (DIC)

Consumptive coagulopathy associated with serious illness.

•Symptoms: Thrombocytopenia, excessive bleeding or clotting

•Diagnosis: Decreased fibrinogen, platelets; increased prothrombin time (PT)/ partial thromboplastin time (PTT), d-dimer test; schistocytes present

•Treatment: Treat underlying cause; platelets and cryoprecipitate for bleeding, low-dose heparin for clotting

Hypercoagulable State

•Risk factors: Prior embolus, pregnancy, surgery, tobacco use, prolonged immobilization, hospitalization, malignancy

•Diagnosis: History and physical examination, complete blood count, PTT

•Treatment: Postoperative patients should be treated for 3 months at an INR of 2 to 3, all others for 3 to 6 months

•Exceptions

– Active cancer: Treat for duration of disease

– Mechanical heart valves: INR goal is 3 to 4

Specific thrombophilic disorders

Disease

Thrombosis

Factor V Leiden

Venous

Protein C/S deficiency

Arterial and venous

Heparin-induced thrombocytopenia (HIT)

Arterial and venous

Anticoagulation medications

Laboratory check

Reversibility

Warfarin

INR

Fresh frozen plasma, vitamin K

Heparin

PTT and platelet count (monitor for HIT)

Protamine

Low-molecular-weight heparin

Antifactor Xa

No

Fondaparinux (factor Xa inhibitors)

No monitoring

No

Dabigatran (direct thrombin inhibitors)

PTT

No

Endocrine Disease

Diabetes Mellitus (DM)

Diagnosis

• Random glucose > 200 mg/dL

• Fasting glucose > 126 mg/dL

• Two-hour glucose > 200 mg/dL (75 gm)

• Hemoglobin A1c (HbA1c) > 6.5

Type 1 DM

Type 2 DM

Symptoms

Polyuria, polydipsia, polyphagia

Mild or none

Stature

Skinny

Obese

Etiology

Autoimmune islet cell destruction

Insulin resistance associated with obesity

Treatment

Insulin therapy, glycemic control, lifestyle management

Oral hypoglycemic, glycemic control, lifestyle management

Complication

Diabetic ketoacidosis

Hyperosmolar nonketotic coma

Chronic complications

Retinopathy, neuropathy, nephropathy, infections, myocardial infarction, cardiovascular disease, stroke

Insulin types

Oral hypoglycemics

Mechanism

Notes

Biguanide (metformin)

Decreases insulin resistance and glucose production

Can cause lactic acidosis, gastrointestinal upset

Sulfonylurea (glyburide)

Stimulates insulin release

Can cause hypoglycemia

Meglitinide (repaglinide)

Stimulates pancreas to release insulin

Can cause weight gain

Thiazolidinedione (pioglitazone)

Decreases insulin resistance peripherally

Causes retention of fluid

Goals of treatment

• BP < 130/85 mm Hg

• Low-density lipoprotein < 100 mg/dL, total glycerides < 150 mg/dL, high-density lipoprotein > 40 mg/dL

• Smoking cessation

• Glycemic control for HbA1c < 7

Monitoring glycemic control in DM

• HbA1c >10 is poor control

• HbA1c between 8.5 and 10 is fair control

• HbA1c between 7 and 8.5 is good control

• Fasting glucose < 130 mg/dL

• Peak postprandial glucose < 180 mg/dL

Diabetic Ketoacidosis

An insulin deficiency and glucagon excess that causes severe hyperglycemia and ketogenesis. Severe hyperglycemia causes an osmotic diuresis leading to dehydration and volume depletion.

•Symptoms: Abdominal pain, nausea, vomiting, Kussmaul respirations, ketone breath, anion gap metabolic acidosis, marked dehydration, tachycardia, polydipsia, polyuria, weakness, altered consciousness

•Diagnosis: Serum glucose > 250 mg/dL, metabolic acidosis (pH > 7.3 and serum bicarbonate < 15 mEq/L), increased anion gap, ketonuria, ketonemia; check chemistry panel for hyperkalemia and hyponatremia

•Treatment:

– IV insulin dose at 0.1 units/kg, then start drip at 0.1 units/kg/hour (check potassium prior to starting insulin); drip should run with normal saline replacement

– Once anion gap has closed and acidosis is resolved, start to decrease the insulin and switch to subcutaneous insulin

– Add dextrose to IV fluids when glucose is below 250 mg/dL

– Manage sodium, potassium, and magnesium levels very closely

Thyroid Disorders

Hypothyroid

Hyperthyroid

Diagnosis

Elevated TSH and decreased T4

Decreased TSH and increased T4

Symptoms

Fatigue, weight gain, cold intolerance, depression

Palpitations, heat intolerance, sweating, anxiety

Examples

Hashimoto thyroiditis, subacute thyroiditis, iodine deficiency

Graves disease, toxic nodule, goiter

Treatment

Synthroid

Ablation surgery, propylthiouracil, methimazole

Complications

Myxedema coma with hypercapnia, hypoventilation, hypothermia

Atrial fibrillation, thyroid storm

TSH, thyroid-stimulating hormone; T4, thyroxine.

Adrenal Disorders (Fig 1-4)

Fig 1-4 Diagnostic algorithm for adrenal disorders. Na, sodium; K, potassium; Ca, calcium; AM, morning; ACTH, adrenocorticotropic hormone.

Complications: Adrenal crisis—shock, nausea, vomiting, confusion, fever; can be fatal

Addison disease (primary adrenal insufficiency)

•Etiology: Autoimmune adrenalitis, malignancy, infection

•Symptoms: Hyperpigmentation of the oral mucosa, dehydration, hypotension, fatigue, anorexia, nausea, vomiting, diarrhea, abdominal pain, salt craving, hyponatremia, hyperkalemia

•Diagnosis: Check chemistry panel for electrolyte abnormalities, low cortisol, high adrenocorticotropic hormone (ACTH)

•Treatment: Mineralocorticoid and glucocorticoid replacement

Cushing syndrome

•Etiology: Exogenous steroids, pituitary adenoma, ectopic ACTH, adrenal hyperplasia

•Symptoms: Moon facies, “buffalo hump,” hypertension, truncal obesity, depression, striae, diabetes, osteopenia, hypokalemia, metabolic acidosis

•Diagnosis: Check chemistry panel for acidosis and abnormalities of electrolytes; conduct dexamethasone suppression test or 24-hour urine free cortisol level

•Treatment: For Cushing syndrome, adenoma resection; if ectopic ACTH release, treat underlying neoplasm

Pituitary Disorders

Hormones released from pituitary gland include: ACTH, thyroid-stimulating hormone (TSH), luteinizing hormone/follicle stimulating hormone (LH/FSH), growth hormone (GH), prolactin.

Hypopituitarism

•Etiology: Invasive disease, infiltrative disease, infarction, head trauma, iatrogenic infection

•Symptoms: Depends on the hormone deficiency; GH, LH/FSH, TSH, ACTH, antidiuretic hormone

•Diagnosis: Blood test for specific hormones suspected in hypopituitarism

•Treatment: Treat the underlying cause and correct hormone deficiencies with appropriate oral/nasal hormonal medications

Hyperpituitarism

•Etiology: Adenoma, prolactinoma

•Symptoms: Headache, vision changes, additional symptoms specific to hormone released from pituitary gland

– Prolactinoma has additional symptoms: Galactorrhea, amenorrhea, impotence

•Diagnosis: MRI, visual field testing for bitemporal hemianopsia (other defects may occur with larger lesions)

•Treatment: Surgical removal of adenoma, dopamine agonists for prolactinomas

Hypercalcemia

•Symptoms

– “Moans” (stupor, depression, psychosis)

– “Groans” (nausea, vomiting, constipation)

– “Stones” (kidney stones, nephrogenic diabetes insipidus)

– “Bones” (arthritis, fractures)

– Other symptoms: Weakness, hypertonia, bradycardia

•Etiology: Malignancy (parathyroid hormone-related protein [PTHrP], local osteolysis), granulomatous disorders, Paget disease

•Diagnosis: Check parathyroid hormone, ionized calcium

•Treatment: Normal saline infusion for urinary excretion

– If calcium is still elevated after normal saline infusion, consider diuretics to inhibit calcium reabsorption and bisphosphonates or calcitonin when hypercalcemia is secondary to malignancy

– Glucocorticoids may be used to treat hypercalcemia in patients with multiple myeloma

Hypocalcemia

•Symptoms: Neuromuscular excitability (seizures, tetany), Chvostek sign, Trousseau sign, prolonged QT interval

•Etiology: Hypoparathyroidism, parathyroid hormone resistance, vitamin D deficiency

•Diagnosis: Check ionized calcium, parathyroid hormone values, renal function

•Treatment: Intravenous calcium drip acutely, oral calcium (calcitriol, if needed) chronically

Autoimmune Disease

Sarcoidosis

•Definition: Autoimmune disease causing noncaseating granulomas

•Etiology: Unknown

•Symptoms: Nonspecific symptoms such as fever, weight loss, arthralgias

•Diagnosis: Biopsy of granulomas, exclusion of other diseases, chest radiograph or computed tomography (CT) scan

– Lip biopsy: Minor salivary glands will show noncaseating granulomas even with normal-appearing mucosal tissue

•Treatment: Systemic steroids

Rheumatoid Arthritis

•Symptoms: Morning pain and stiffness, erythema and warmth in joint, symmetric pattern, presence of rheumatoid nodules, ulnar deviation of metacarpophalangeal joints, swelling of the proximal interphalangeal joints, swan neck deformity, boutonnière deformity

•Diagnosis: Rheumatoid factor titers, classic radiologic findings, elevated erythrocyte sedimentation rate and C-reactive protein, anti-citrullinated protein antibody present

– Can be associated with serositis, ocular disease, amyloidosis, atherosclerosis

– Firm diagnosis requires at least 6 points from criteria for rheumatoid arthritis classification

Criteria for rheumatoid arthritis classification

Description

Points

Joint involvement

1 large joint

2–10 large joints

1–3 small joints

4–10 small joints

> 10 joints

0

1

2

3

5

Serology

–RF and –ACPA

+RF or low +ACPA

+RF or high +ACPA

0

2

3

Acute phase reactants

Normal CRP and ESR

Elevated CRP or ESR

0

1

Duration

< 6 weeks

≥ 6 weeks

0

1

RF, rheumatoid factor; ACPA, anti-citrullinated protein antibody; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate.

Rheumatoid arthritis versus osteoarthritis

•Treatment: Disease-modifying antirheumatic drugs such as methotrexate or a tumor necrosis factor alpha (TNF-alpha) inhibitor

Systemic Lupus Erythematosus

•Symptoms: Arthralgias, photosensitive rash (malar region is common), oral ulcers, pancytopenia, serositis

•Diagnosis: Anti–double standard DNA (anti-dsDNA), antinuclear antibody (ANA) testing, anti-Smith antibodies, antiphospholipid antibodies

•Treatment

– Sun avoidance/protection, nonsteroidal anti-inflammatory drugs (NSAIDs)

– Increasing doses of systemic steroids based on disease severity

– Severe disease requires IV chemotherapeutic agents such as cyclophosphamide, azathioprine, rituximab

Myasthenia Gravis

•Definition: Autoimmune disorder with auto-antibodies to acetylcholine receptor

•Symptoms: Fluctuating, fatigable weakness classically affecting the eye muscles causing ptosis, extraocular muscle palsies, easy fatigability of proximal muscles, preserved deep tendon reflexes

•Diagnosis: Anti-nicotinic acetylcholine receptor (anti-nAChR) antibodies, anti-muscle-specific tyrosine kinase (anti-MuSK) antibodies, Tensilon (Hoffmann-LaRoche) test, electromyography (EMG)

•Treatment

– Anticholinesterase inhibitors (ie, physostigmine)

– Immunomodulators

– Thymectomy; thought to reduce autoantibody production

•Complication: Myasthenic crisis leading to respiratory failure

– Treat with IV immunoglobulin/plasmapheresis

– May require temporary intubation

Sclerosing Syndromes

Allergy

Vasculitides

Serology Tests

Disease association

ANCA

Wegener granulomatosis

Anti-dsDNA

Lupus erythematosus

ANA

• Rheumatoid arthritis

• Lupus erythematosus

• Sjögren syndrome

• Diffuse and limited scleroderma

• Myositis

• Wegener granulomatosis

Anti-SSA

• Sjögren syndrome

• Lupus erythematosus

Anti-SSB

• Sjögren syndrome

• Lupus erythematosus

RF

• Rheumatoid arthritis

• Lupus erythematosus

• Sjögren syndrome

• Diffuse and limited scleroderma

• Myositis

• Wegener granulomatosis

ANCA, antineutrophil cytoplasmic antibodies; anti-SSA, anti–Sjögren syndrome A; anti-SSB, anti–Sjögren syndrome B; RF, rheumatoid factor.

Neurologic Disorders

Syncope

Transient loss of consciousness and postural tone.

•Symptoms: Paleness, lightheadedness, sweating, nausea

•Diagnosis: History and physical examination with vital signs, ECG, Holter monitoring, tilt-table testing

•Treatment: Treat underlying condition (always initially search for cardiac etiology)

Seizure

Abnormal discharge of cortical neurons.

Primary generalized seizures

• Tonic-clonic: Associated with urinary incontinence, postictal confusion

• Myoclonic: Abrupt contraction of a single muscle group

•Diagnosis: Lab tests to evaluate electrolytes, brain magnetic resonance imaging (MRI), electroencephalogram (EEG)

•Treatment: Broad-spectrum anticonvulsants

Focal seizures

• Simple: No loss of consciousness but symptoms of twitching/jerking

• Complex focal: Impairment of consciousness develops, causing automatisms

• Complex focal with secondary generalization: Spreads to involve the cerebral cortex

•Diagnosis: EEG, brain imaging

•Treatment: Anticonvulsants, surgery

Static epilepitus

• Continuous seizure activity > 30 minutes or recurrent seizures without return of consciousness

•Treatment: Check airway, breathing, circulation; draw blood for lab tests; consider thiamine, glucose, benzodiazepines, phenytoin

Cerebrovascular Accident

Acute onset focal neurologic changes secondary to blood flow disruption to the brain.

Ischemic stroke

Emboli from internal carotid artery or heart causing blood vessel blockage.

•Diagnosis: Noncontrast head CT scan

•Treatment: Tissue plasminogen activator if < 3 hours from stroke symptom onset, antiplatelet medications, statins, blood pressure control

Hemorrhagic stroke

Associated with headache and rapid loss of consciousness, with hypertension being primary cause.

•Diagnosis: Noncontrast head CT scan

•Treatment: Supportive care, endovascular procedures, open surgery to stop bleeding

Intracranial Bleeding

Declined Mental Ability

Dementia

Delirium

Definition

Acquired syndrome with slow decline in memory and cognition

Rapid-onset confusion and disorientation with fluctuating intensity

Etiology

Alzheimer, Lewy body dementia, medications, metabolic disorders, vascular infarction, chronic disease

Elderly hospitalized patients with risk factors including infection, depression, fever

Symptoms

Personality changes, trouble with activities of daily living, impaired judgment

Waxing and waning alterations in consciousness and cognition

Diagnosis

Mini-mental status exam, CBC, electrolytes, creatinine, liver function tests, TSH/B12 levels, rapid plasmin regain test, HIV test

Physical exam with same lab tests as for dementia

Treatment

Treat underlying cause, antidepressants, antipsychotics

Behavioral and environmental change, low-dose haloperidol if needed

CBC, complete blood count.

Neuroleptic Malignant Syndrome

•Etiology: Decreased levels of dopamine activity secondary to dopamine receptor blockade

•Symptoms: Increased body temperature, altered consciousness, diaphoresis, rigid muscles, autonomic imbalance

•Treatment: Stop neuroleptic drugs, treat hyperthermia. intensive care unit care, dantrolene for muscle rigidity, intravenous fluids

Serotonin Syndrome

•Etiology: Excess of serotonergic activity in the central nervous system and peripheral serotonin receptors from therapeutic drug use, recreational drug use, or drug interactions

•Symptoms: Headache, agitation, confusion, shivering, sweating, hyperthermia, hypertension, tachycardia, nausea, vomiting, hyper-reflexia, tremors, muscle twitching

•Treatment: Stop drugs, give serotonin antagonists, supportive care for sympathetic hypersensitivity and concomitant symptoms

Differentiating Serotonin Syndrome from Neuroleptic Malignant Syndrome

Serotonin syndrome

Neuroleptic malignant syndrome

Onset

24 hours

Days to weeks

Causative agent

Serotonin agonist

Dopamine antagonist

Muscular findings

Excitability

Rigidity

Treatment

Serotonin antagonist and benzodiazepines

Dopamine agonist and dantrolene

Resolution

Within 24 hours

Days to weeks

Alcohol Withdrawal

Alcohol is a central nervous system depressant that enhances gamma-aminobutyric acid (GABA) inhibitory tone and inhibits excitatory amino acid activity. Abrupt removal of alcohol results in overactivity of the central nervous system.

•Symptoms: Anxiety 2 to 3 days after last drink; sympathetic hyperactivity and hypersensitivity; delirium tremens 36 hours after last drink

• Delirium tremens: Hypertension, tachycardia, agitation, hyperthermia

Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol

To assess the level of withdrawal and medication needed, use the CIWA protocol. The CIWA protocol has 10 categories noted below, with scoring of 0 to 7 in all categories except orientation, which is scored 0 to 4.

• Nausea/vomiting

• Anxiety

• Visual disturbance

• Paroxysmal sweats

• Tactile disturbance

• Orientation

• Auditory disturbance

• Headache

• Agitation

• Tremors

Score

Withdrawal

Less than 8

Prophylaxis

8–15

Mild

16–25

Moderate

> 25

Severe

General treatment

• Hydration

• Correct electrolyte imbalance

• Thiamine, 100 mg IV daily for 3 days, then orally daily

• Folic acid, 1 mg orally daily

• Benzodiazepine taper (long-acting preferred for smoother withdrawal course and smaller chance of seizures or recurrent withdrawal symptoms)

Parkinson Disease

Progressive, idiopathic disease.

•Symptoms: Resting tremor, bradykinesia, cogwheel rigidity, postural instability; symptoms begin asymmetrically

•Pathology: Affects the dopamine neurons of the substantia nigra

•Treatment: Levodopa/carbidopa, dopamine agonists, anticholinergics

Huntington Disease

Progressive, autosomal dominant disease (cytosine-adenine-guanine expansion in DNA).

•Symptoms: Chorea, dementia, psychiatric symptoms

•Pathology: Atrophy of the caudate nucleus

•Treatment: None available

Alzheimer Disease

•Etiology: Unknown but genetic component may be present; low levels of acetylcholine

•Pathology: Senile plaques with central amyloid core and bundles of neurofilaments in neuronal cytoplasm

•Symptoms: Mild forgetfulness with poor concentration and changes in personality that worsen in later stages to paranoid delusions, hallucinations, and need for assistance in all activities of daily living

•Treatment: Avoid anticholinergics; donepezil is a first-line agent.

Lewy Body Dementia

•Etiology: Loss of cholinergic neurons and death of dopaminergic neurons

•Pathology: Lewy bodies (alpha synuclein cytoplasmic inclusions) present in the cortex

•Symptoms: Variation in cognition and attention; recurrent hallucinations and Parkinson-like motor symptoms

•Treatment: Donepezil for cognition and levodopa for motor symptoms; otherwise, palliation

Perioperative Management

Shock

Pathophysiologic state associated with decreased tissue perfusion and hypoxia.

Categories

Stages of shock

Reversible

Definition

Initial

Yes

No signs of shock but cells starting to use anaerobic metabolism

Compensatory

Yes

Compensatory mechanisms try to reverse the symptoms of shock (eg, hyperventilation to correct acidosis)

Progressive

No

Compensatory mechanisms cannot correct shock symptoms, leading to worsening acidosis and decreased organ perfusion

Refractory

No

Organ failure and death

Treatment

• Aggressive IV fluid hydration with initial 2 L bolus (except in cardiogenic shock)

• Cardiogenic shock: Decrease afterload, increase cardiac output, decrease myocardial oxygen demand

• Treat underlying cause

Classes of hemorrhage

Postoperative Fever

Postoperative day

Cause

1–2

Wind (pneumonia)

3–5

Water (urinary tract infection)

4–6

Walking (deep vein thrombosis/pulmonary embolism)

5–7

Wound (surgical site infection)

> 7

Wonder drugs (drug fever)

Treatment

• Physical examination

• Complete blood count (CBC) with differential count

• Panculture the patient

• Replace all lines

• Review old culture results

• Lower extremity Doppler study

• Chest radiograph

Common Perioperative Issues

Fluid management

Maintenance

• Follow the 4/2/1 rule for maintenance fluid management

– 4 cc/kg for the first 10 kg

– 2 cc/kg for the second 10 kg

– 1 cc/kg for each kg thereafter

• Additional fluid infusion for instances such as

– Fever

– Drains

– Gastrointestinal losses

– Burns

• Decreased fluid infusion for instances such as

– Edematous states

– Hypothyroidism

– Renal failure

Hypovolemia

• Colloid versus crystalloid therapy

– Crystalloid therapy is the gold standard except in cases of severe blood loss; begin therapy with 2 liters of isotonic crystalloid fluid

– Colloid therapy is more expensive and has not shown a benefit over crystalloid therapy

• Blood transfusion

– Use in cases of severe hemorrhagic hypovolemia or hemorrhagic shock

Postoperative fluid overload

• Signs include pitting edema, hypertension, lung crackles, shortness of breath, increased jugular vein distention

• Treatment

– Fluid restriction

– Sodium restriction

– Diuretic therapy

– Monitor urine output

– Reposition patient to decrease dependent collection of fluids

Cardiovascular management

This is discussed in detail in the cardiovascular section (see page 2).

Beta blockers

• High-risk patients may benefit from preoperative beta blockade, but careful monitoring for appropriate heart rate and blood pressure is critical

• Choice of beta blocker should be discussed with cardiologist or medical consult team; usually selective beta-1 blockade is preferred

Hypertension

• Ensure patient is taking preoperative medications

• Look for other causes (pain, bladder distension, hypoxia, hypervolemia)

• For new onset postoperative hypertension without an underlying cause, consider nitroprusside or labetolol and speak to cardiologist regarding further management

Atrial fibrillation

• Rule out thyroid disease, systemic illness, pulmonary embolus, and acute myocardial infarction

• Symptoms include palpitations, dizziness, irregularly irregular pulse

• ECG will show a wavy baseline with loss of P waves

• Acute-onset atrial fibrillation in an unstable patient requires immediate electrical cardioversion

• Acute-onset atrial fibrillation in a stable patient requires rate control with beta blockers and calcium channel blockers

– Once rate control is achieved, cardioversion is required to convert patient back to normal sinus rhythym

– If the arrhythmia has been present for more than 48 hours, anticoagulation is required for 3 weeks before and 4 weeks after cardioversion

– Earlier cardioversion is done if no thrombus is present on transesophageal echocardiogram

Chest pain

• ECG (ST elevations, T wave changes, Q waves for acute myocardial infarction diagnosis)

• Chest radiograph

• Test for troponins and creatine kinase-MB (will elevate 6–8 hours post chest pain onset)

• Supplemental oxygen

• Speak to cardiologist regarding therapy for ischemic heart disease

– Beta blockers

– Aspirin

– Nitroglycerin

– Heparin therapy

• Cardiac catheterization for high-risk patients (STEMI)

• Cardiac stress testing for low-risk patients

Pulmonary management

Acute respiratory distress syndrome

• Hypoxemic respiratory failure with bilateral lung infiltrates

• No evidence of heart failure

– Symptoms include tachypnea and diffuse lung crackles

– Chest radiograph will show bilateral alveolar infiltrates

– Pulmonary wedge pressure is less than 18 mm Hg

– Partial pressure of oxygen (PaO2)/fractional inspired oxygen (FiO2) is less than 200 mm Hg

– If PaO2/FiO2 is between 200 and 300 mm Hg, diagnosis is acute lung injury

• Treatment

– Treat underlying cause

– Low tidal volumes (6 cc/kg)

– Low PEEP

– Conservative fluid management

– Plateau pressure less than 30 cm H2O

Postoperative respiratory failure

• Asthma

– Supplemental oxygen

– Short-acting beta agonist

– Systemic steroids

– IV magnesium sulfate

• Pulmonary embolus

– Supplemental oxygen

– Heparin therapy

• Guillain-Barré syndrome

– Supplemental oxygen

– Mechanical ventilation

– Plasmapheresis or IV immunoglobulin infusion

• Pneumonia

– Culture sputum

– Empiric therapy with Unasyn (Pfizer) or Zosyn (Pfizer)

Epilepsy

Postoperative status epilepticus

• Prolonged and sustained loss of consciousness

• Persistent convulsions

• Look for organic cause and rule out metabolic disorder, neoplasm, intracranial infection, stroke, drug intoxication

• Treatment

– Establish airway

– Establish IV access

– STAT labs (CBC, electrolytes, liver panel, anticonvulsant medication level)

– IV benzodiazepines (diazepam)

– Loading dose of anticonvulsant medication

∘ IV dextrose

∘ IV thiamine

Diabetes management

Patient on insulin

• Preoperative: Give 50% long-acting insulin dose on morning of surgery; start IV glucose drip

• Postoperative: Start IV glucose drip

Patient not on insulin

• Preoperative: Discontinue oral hypoglycemics and metformin 24 hours preoperatively

• Postoperative: Insulin drip with a short-acting sliding scale

Steroid management

Patients taking steroids chronically

• Daily dose of 20 mg or more of prednisone or equivalent

• More than 3 weeks of steroid treatment

• An acute cortisol deficiency secondary to surgical stress, in a patient with adrenal insufficency, will lead to adrenal crisis; symptoms include headache, nausea, vomiting, shock, and confusion; without steroid dosing, this can be fatal

Treatment: Steroid stress dosing

Antibiotic prophylaxis

Conditions that require prophylaxis for oral procedures

• Prosthetic cardiac valve

• Prosthetic material for cardiac valve repair

• History of infective endocarditis

• Congenital heart disease (CHD)

– Unrepaired cyanotic CHD

∘ Completely repaired congenital defect with prosthetic material or device within 6 months of repair

– Repaired CHD with residual disease

∘ Cardiac transplant patients who have developed valvulopathy

• No antibiotic prophylaxis is required for dialysis patients or patients who have had joint replacement or solid organ transplants unless otherwise specified by their doctors

Recommended Readings

Abubaker AO, Benson KJ (eds). Oral and Maxillofacial Surgery Secrets, ed 2. St Louis: Mosby, 2007:157–226.

Ali RY, Reminick MS. Perioperative management of patients who have pulmonary disease. Oral Maxillofac Surg Clin North Am 2006;18:81–94.

Ansari R. Fever work-up and management in postsurgical oral and maxillofacial surgery patients. Oral Maxillofac Surg Clin North Am 2006;18:73–79.

Bergman SA. Perioperative management of the diabetic patient. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:731–737.

Carrasco LR, Chou JC. Perioperative management of patients with renal disease. Oral Maxillofac Surg Clin North Am 2006;18:203–212.

Chacon GE, Ugalde CM. Perioperative management of the patient with hematologic disorders. Oral Maxillofac Surg Clin North Am 2006;18:161–171.

Clarkson E, Bhatia SR. Perioperative management of the patient with liver disease and management of the chronic alcoholic. Oral Maxillofac Surg Clin North Am 2006;18:213–225.

Dubin D. Rapid Interpretation of EKG’s: An Interactive Course, ed 6. Tampa: Cover, 2000.

Halpern LR, Feldman S. Perioperative risk assessment in the surgical care of geriatric patients. Oral Maxillofac Surg Clin North Am 2006;18:19–34.

Laskin DM. Clinician’s Handbook of Oral and Maxillofacial Surgery. Chicago: Quintessence, 2010.

Le T, Bhushan V, Bagga HS. First Aid for the USMLE Step 3, ed 3. New York: McGraw Hill Medical, 2011.

Marino PL, Sutin KM. Acid-Base Disorders. In: Marino PL, Sutin KM (eds). The ICU Book, ed 3. Philadelphia: Lippincott Williams & Wilkins, 2006:559–605.

Marino PL, Sutin KM. Hypertonic and hypotonic conditions. In: Marino PL, Sutin KM (eds). The ICU Book, ed 3. Philadelphia: Lippincott Williams & Wilkins, 2006:622–638.

Marino PL, Sutin KM. Potassium. In: Marino PL, Sutin KM (eds). The ICU Book, ed 3. Philadelphia: Lippincott Williams & Wilkins, 2006:639–654.

Ogle OE. Gastrointestinal diseases and considerations in the perioperative management of oral surgical patients. Oral Maxillofac Surg Clin North Am 2006;18:241–254.

Ogle OE. Postoperative care of oral and maxillofacial surgery patients. Oral Maxillofac Surg Clin North Am 2006;18:49–58.

Sinz E, Navarro K, Soderberg ES, Callaway CW. Advanced Cardiovascular Life Support: Provider Manual. Dallas: American Heart Association, 2011.

Chapter 2

Anesthesia

Jason Jamali and Stuart Lieblich

Basic Patient Preanesthesia ManagementPharmacologyMechanical VentilationPerioperative CareAnesthesia for Special Populations

Basic Patient Preanesthesia Management

Preoperative Airway Evaluation

• Mandibular opening (> 3 finger)

• Dentition

• Thyromental distance (> 6 cm)

• Cervical spine (35 degrees of neck extension)

• Neck (scars from previous surgeries)

• Mallampati classification

1. Soft/hard palate, uvula, tonsillar pillars visible

2. Soft/hard palate, parts of uvula visible (tonsillar pillars not visible)

3. Soft/hard palate, base of uvula visible

4. Hard palate only visible

• Preoperative testing: Consider complete blood count (CBC), electrolytes, coagulation studies, pregnancy test, electrocardiogram (ECG) (age > 50 and/or general anesthesia), chest radiograph depending on the type of surgery

Preoperative Fasting Guidelines

Ingested material

Minimum fasting period (hours)

Clear liquids

2

Breast milk

4

Infant formula

6

Nonhuman milk

6

Light meal

6

Heavy meal

8+

American Society of Anesthesiologists (ASA) Classification

   I:

Normal healthy patient

  II:

Mild-moderate systemic disease

 III:

Severe systemic disease

 IV:

Severe systemic disease that is a constant threat to life

  V:

Moribund patient not expected to survive without surgery

VII:

Declared brain dead, planned for organ harvest

  E:

Any emergency

Perioperative Monitoring

Pulse oximetry

• Monitors oxygen saturation of hemoglobin and heart rate

• Sources of error: Shivering, fingernail polish, carboxyhemoglobin, methemoglobin, methylene blue, hypothermia, hypotension, hypovolemia, hypoxia, ambient light

ECG

• Used for identification of dysrhythmias, myocardial ischemia, pacemaker function

• Leads II and V5 are commonly used—more sensitive to ischemia

Blood pressure

• Noninvasive blood pressure monitoring reflects blood flow, whereas invasive monitoring is more directly correlated with blood pressure and allows for real-time continuous monitoring via placement of an intra-arterial catheter

• Invasive blood pressure monitoring is indicated in patients that are hemodynamically unstable, undergoing major surgery where a higher blood loss is anticipated, receiving vasoactive medications, or requiring frequent lab draws

• Due to gravity, blood pressure in the lower extremities may be higher

•Source of error: Improper size cuff will give inaccurate results

– Too large of a cuff: Falsely low blood pressure

– Too tight of a cuff: Falsely elevated blood pressure

Capnography

• Carbon dioxide measurement allows for

– Assessment of ventilation

– Assessment of circulation

– Verification of intubation

– Identification of anesthetic circuit malfunction (eg, leaks, disconnection)

Bispectral index (BIS)

• Objectively measures the depth of anesthesia (intravenous or inhalational)

• Mechanism

– Uses electroencephalogram (EEG) data obtained via scalp electrodes to calculate a depth of anesthesia represented by a dimensionless number between 0 and 100

– Deeper levels of anesthesia are represented by lower numbers

• Should be used only as an adjunct to evaluation as several sources of error exist

– Paradoxic changes with certain anesthetics (ketamine, N20)

– Electrical device interference (electrocautery)